Volume 26, Issue 1 pp. 55-62

Human cytomegalovirus infection inhibits response of chronic hepatitis-C-virus-infected patients to interferon-based therapy

Noha G Bader El Din

Noha G Bader El Din

Department of Biomedical Technology, National Research Center, Cairo, Egypt,

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Mai Abd El Meguid

Mai Abd El Meguid

Department of Biomedical Technology, National Research Center, Cairo, Egypt,

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Ashraf A Tabll

Ashraf A Tabll

Department of Biomedical Technology, National Research Center, Cairo, Egypt,

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Mohamed A Anany

Mohamed A Anany

Department of Biomedical Technology, National Research Center, Cairo, Egypt,

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Gamal Esmat

Gamal Esmat

Department of Tropical Medicine, Faculty of Medicine Cairo University, Cairo, Egypt,

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Naglaa Zayed

Naglaa Zayed

Department of Tropical Medicine, Faculty of Medicine Cairo University, Cairo, Egypt,

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Amr Helmy

Amr Helmy

Department of Surgery, National Liver Institute, Menoufia University, Menoufia, Egypt

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Abdel Rahman El Zayady

Abdel Rahman El Zayady

Department of Internal Medicine, Faculty of Medicine, Ain Shams University, Cairo, Egypt,

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Ahmed Barakat

Ahmed Barakat

Department of Microbiology, Faculty of Science, Ain Shams University, Cairo, Egypt, and

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Mostafa K El Awady

Corresponding Author

Mostafa K El Awady

Department of Biomedical Technology, National Research Center, Cairo, Egypt,

Dr Mostafa El-Awady, Department of Biomedical Technology, National Research Center, El-Behooth Street 12622, Dokki, Giza, Egypt. Email: [email protected]Search for more papers by this author
First published: 22 December 2010
Citations: 21

Abstract

Background and Aim: Cytomegalovirus (CMV) is a ubiquitous pathogen that infects the majority of humans. Co-infection of CMV and hepatitis C virus (HCV) may deteriorate the prognosis of HCV-infected patients. This study was conducted to examine the role of CMV reactivation in determining the response rate to treatment with interferon and ribavirin therapy in chronic HCV patients.

Methods: Viral loads and genotyping were assessed using reverse transcription polymerase chain reaction and Innolipa systems, respectively. Reactivation of CMV in HCV patients who were all positive for CMV immunoglobulin G antibodies was tested by amplification of the gB1 gene using the end-point dilution quantitative-nested polymerase chain reaction method.

Results: CMV DNA was detected in 89.7% of non-responders and in 34.6% of sustained virological responders. Patients with reactivated CMV had significantly higher fibrosis scores (72.7%) than those with undetectable CMV DNA (23.8%, P = 0.002). Patients with positive CMV had higher rates of non-response and relapse (79.5%) than those with negative CMV DNA (19%). Chronic HCV patients with latent CMV had higher rates of response (81%) to treatment than those with reactivated CMV (20.5%, P < 0.001). Therefore, HCV patients with reactivated CMV and advanced fibrosis were least likely to achieve a sustained virological response following interferon therapy. This possibility is reduced to 50% of its original value in patients with reactivated CMV without fibrosis.

Conclusions: Besides the staging of liver fibrosis, CMV co-infection should be considered as an extremely important factor when designing predictive models for HCV response to interferon treatment.

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